Red cell distribution width is a potential predictor of early relapse in polymyalgia rheumatica.

Red blood cell distribution width (RDW) has been studied as a prognostic biomarker for different chronic inflammatory diseases. In this paper we aim to evaluate its potential role in the prediction of early relapse in patients affected by polymyalgia rheumatica (PMR). We revised retrospectively clinical records of patients who received a diagnosis of PMR, according to 2012 ACR/EULAR classification criteria, for whom baseline clinical and laboratory data were available. The baseline RDW variation coefficient was correlated to the risk of relapse, in the first 6 months of the disease. We identified 44 patients [females 15 (34.0%)/males 29 (66.0%); median age 80 (72-83)], 9 of whom had an early relapse. These patients showed a larger median RDW than patients who did not relapse [13.7 (13.5-14.9)% vs 13.5 (12.7-14.2)%; p=0.04). The two groups were comparable for all the other clinical and laboratory parameters considered. Interestingly, patients in the higher half of the RDW distribution showed a shorter relapse-free survival (p<0.03). In a stepwise logistic regression, RDW (p=0.01) predicted the risk of relapse at 6 months, while age, gender, CRP, ESR, Hb, MCV and prednisone dose did not fit the model. Our results show that RDW is an independent biomarker of early relapse, making this parameter a potentially promising predictive marker in PMR.

Association between red cell distribution width and response to methotrexate in rheumatoid arthritis.

Red cell distribution width (RDW) is an unconventional biomarker of inflammation. We aimed to explore its role as a predictor of treatment response in rheumatoid arthritis (RA). Eighty-two RA patients (55 females), median age [interquartile range] 63 years [52-69], were selected by scanning the medical records of a rheumatology clinic, to analyze the associations between baseline RDW, disease activity scores and inflammatory markers, as well as the relationship between RDW changes following methotrexate (MTX) and treatment response. The lower the median baseline RDW, the greater were the chances of a positive EULAR response at three months, 13.5% [13.0-14.4] being among those with good response, vs 14.0% [13.2-14.7] and 14.2% [13.5- 16.0] (p=0.009) among those with moderate and poor response, respectively. MTX treatment was followed by a significant RDW increase (p<0.0001). The increase of RDW was greater among patients with good EULAR response, becoming progressively smaller in cases with moderate and poor response (1.0% [0.4-1.4] vs. 0.7 [0.1-2.0] vs. 0.3 [-0.1-0.8]; p=0.03). RDW is a strong predictor of early response to MTX in RA. RDW significantly increases after MTX initiation in parallel to treatment response, suggesting a role as a marker of MTX effectiveness.

Inflammatory markers predict insulin sensitivity in active rheumatoid arthritis but not in psoriatic arthritis.

Whether the insulin resistance commonly observed in patients with inflammatory arthritis is a disease-specific feature and/or is limited to a disease phase (i.e., it occurs only during phases of high disease activity) is unknown. Fifty-three rheumatoid arthritis (RA) and 44 psoriatic arthritis (PsA) patients were recruited consecutively along with 194 controls matched for age, sex and body mass index for a case-control study. All underwent an oral glucose tolerance test, the results of which were analysed to derive the following indexes: homeostatic model of insulin resistance (HOMA-IR), insulin sensitivity index (ISI) and early insulin sensitivity index (EISI). These data were related to anthropometric, clinical and laboratory findings. Metabolic parameters of patients and controls were similar. Neither inflammatory markers nor disease activity scores were related to glucose metabolism for the generality of RA and PsA patients; however, by restricting the analysis to the subset of RA patients with residual disease activity, an association emerged between erythrocyte sedimentation rate, on the one hand, and fasting insulin (ß=0.46, p=0.047) and HOMA-IR (ß=0.44, p=0.02), on the other. Moreover, C-reactive protein (CRP) levels were associated with plasma glucose and insulin levels measured 120 min after the glucose load (ß=0.91, p=0.0003 and ß=0.77, p=0.0006, respectively); ISI and EISI were predicted by CRP (ß=-0.79, p=0.0006; ß=-0.80, p=0.0001, respectively). The same did not hold true for PsA patients. The association between systemic inflammation and insulin resistance indexes is a feature of RA with residual disease activity, not a universal feature of inflammatory arthritides.

ApoB/apoA-I ratio is better than LDL-C in detecting cardiovascular risk.

BACKGROUND AND AIMS: Cardiovascular (CV) events occur even when LDL-C are <100mg/dL. To improve the detection of CV risk we investigated the apoB/apoA-I ratio versus LDL-C in subjects considered normal glucose tolerant (NGT) by oral glucose tolerance test (OGTT). METHODS AND RESULTS: We enrolled 616 NGT (273 men and 343 women), and we measured insulin resistance, lipid profile, apoB/apoA-I and the factors compounding the metabolic syndrome (MetS). An unfavourable apoB/apoA-I (≥0.9 for males and ≥0.8 for females) was present in 13.9% of 108 patients with LDL-C <100mg/dL: compared to subjects with lower apoB/apoA-I (<0.9 for males and <0.8 for females), they had more elements of MetS and their lipid profile strongly correlated with high CV risk. Out of 314 patients with lower apoB/apoA-I, 40.12% had LDL-C ≥130mg/dL: these retained a more favourable lipid profile than corresponding subjects with elevated apoB/apoA-I ratio. Finally, we found a significant correlation between LDL-C and apoB/apoA-I ratio (r=0.48, p<0.0001). CONCLUSIONS: In NGT with LDL-C <100mg/dL, a higher apoB/apoA-I exhibited an atherogenic lipid profile, indicating that LDL-C alone is insufficient to define CV risk. Independent from LDL-level, when apoB/apoA-I is lower, the lipid profile is, in fact, less atherogenic. This study demonstrates that apoB/apoA-I is at least complementary to LDL-C in identifying the "effective" CV risk profile of asymptomatic NGT subjects.

Individuation of different metabolic phenotypes in normal glucose tolerance test.

Based on the hypothesis that a more efficient glucose utilization lowers the risk of progression to type 2 diabetes, we tested the capability of oral glucose tolerance test (OGTT) to identify subjects at risk included inside normal glucose tolerance (NGT). We measured fasting and 2-h plasma glucose (FPG and 2hPG) and insulin values (FPI and 2hPI) in 623 normal OGTTs. Insulin sensitivity and secretion were computed with HOMA2 method and Stumvoll's formula. Secretion was expressed as HOMA2%beta, first (1stPH) and second-phase (2ndPH) insulin release. The percentage increment of 2hPG with respect to FPG (PG%) was used to subdivide patients into PG% tertiles, considered as the primary grouping variable. Covariance analysis (ANCOVA) for multiple comparisons was performed considering the above measurements as dependent variables, sex, age, body mass index (BMI) and waist circumference as covariates. In subjects with PG% < or =0, we documented significant increments of insulin sensitivity and significant decrements of resistance and secretion compared to subjects with PG% >0. ANCOVA disclosed that insulin sensitivity fell, while 1stPH secretion rose significantly from the lower to the higher tertile of PG%. OGTT may be useful to establish NGT as well as a more subtle metabolic phenotype. The closer 2hPG is to FPG, the higher insulin sensitivity and the lower insulin secretion are. The stimulus to maintain NGT elicits more insulin secretion, predisposing to worsening glucose tolerance when a faltering insulin secretion ensues. These subjects could benefit from prospective prevention treatment and studies.

[Isolated ACTH deficiency and transient GH deficiency. Presentation of a case]. / Deficit isolato di ACTH e transitorio deficit di GH. Presentazione di un caso.

In a 46 year old man, who arrived at our observation suffering for three months from considerable increasing weakness and progressive impairment of libido, we documented a condition of secondary hypocorticism due to an isolated ACTH deficiency associated with a reduced somatotropin reserve, the last improved after treatment with corticosteroids. We found low serum levels of ACTH and cortisol, good response of adrenal glands to corticotropin depot, normalization of the clinical board during glucocorticoid replacement. Stimulating test with CRH (corticotropin releasing hormone) did not cause a response in ACTH, suggesting the presence of primitive damage of the hypophyseal corticotroph cells.